Ch 18/19 Extended Review

Heart: size and location

About the size of a closed fist; located in the mediastinum of the thoracic cavity

Heart: base vs. apex

Base = wider superior portion; apex = the pointed inferior tip

Fibrous pericardium

Tough, inelastic outer sac; rests on/attached to the diaphragm; anchored to vessels at the heart's base; prevents overfilling of the chambers

Layers surrounding the heart, inside to outside

Endocardium, myocardium, epicardium (visceral serous pericardium), pericardial cavity, parietal serous pericardium, fibrous pericardium

Parietal (outer) serous pericardium

Simple squamous epithelium bound to the fibrous pericardium; secretes lubricating serous fluid

Visceral (inner) serous pericardium

= the epicardium; simple squamous epithelium bound to the myocardium; reduces friction as the heart twists/contracts

Pericarditis

Inflammation of the pericardium; painful, can damage the myocardium

Cardiac tamponade

Fluid buildup or bleeding into the pericardial cavity that compresses the heart and can cause cardiac failure

Heart wall: 3 layers

Epicardium (outer), myocardium (middle, muscle mass), endocardium (inner lining, continuous with vessel endothelium)

Cardiac muscle cell traits

Involuntary, striated, branched; uses the sliding filament mechanism of contraction

Intercalated discs

Junctions connecting cardiac muscle fibers; contain gap junctions and desmosomes

Gap junctions (cardiac)

Allow action potentials to pass directly from one muscle fiber to the next

Desmosomes (cardiac)

"Spot welds" that keep cardiac fibers from pulling apart during contraction

Atrioventricular groove

External landmark separating the atria from the ventricles

Interventricular sulcus

External landmark (anterior/posterior) separating the right and left ventricles; coronary vessels run in these grooves

Left coronary artery branches

Circumflex artery and anterior interventricular artery

Right coronary artery branches

Right marginal artery and posterior interventricular artery

Anastomosis (coronary)

A junction/crosslink between vessels providing collateral circulation (backup routes) if one path is blocked

Coronary sinus

Collects deoxygenated blood from the coronary veins and returns it to the right atrium

When does the myocardium get most of its blood flow?

During diastole, when the heart muscle is relaxed and not compressing the coronary vessels

Minimum blood flow the heart can survive on

10-15% of normal arterial flow

Ischemia vs. hypoxia

Ischemia = decreased blood supply to tissue; hypoxia = low oxygen supply to tissue

Angina pectoris

Chest pain from temporary myocardial ischemia, often during exertion; may radiate to arm, back, neck, or jaw

Myocardial infarction (MI)

Heart attack; a thrombus/embolus blocks a coronary artery, killing tissue distal to the blockage (replaced by scar tissue if patient survives)

Reperfusion damage

Re-establishing blood flow after a blockage can itself damage tissue via oxygen free radicals attacking proteins, membranes, and nucleic acids

Interatrial vs. interventricular septum

Interatrial septum separates the two atria; interventricular septum separates the two ventricles

Full path of blood through the heart

RA -> tricuspid valve -> RV -> pulmonary valve -> pulmonary trunk -> lungs -> pulmonary veins -> LA -> mitral valve -> LV -> aortic valve -> aorta

Heart valve structure

Dense connective tissue flaps covered by endocardium

General valve mechanism

Purely passive: a valve opens when pressure is lower in the chamber ahead of it, and closes when pressure rises behind it

AV valves

Separate atria from ventricles: bicuspid/mitral (left side), tricuspid (right side); have feathery cusp edges

Chordae tendineae & papillary muscles

Chordae tendineae connect AV valve cusps to papillary muscles; papillary muscle contraction keeps the valves from being pushed open backward as ventricular pressure rises

Semilunar valves

Aortic and pulmonary valves; located where blood exits the ventricles into the great arteries; prevent backflow into the ventricles

Valve pathologies

Incompetent = doesn't close properly (leaks/backflow); stenosis = doesn't open properly (hardened/calcified)

Intracellular vs. extracellular ion concentrations (cardiac cells)

Intracellular: high K+; Extracellular: high Na+ and Ca2+

SA node

The heart's pacemaker; located in the right atrium; fires spontaneously at 60-100 beats/min, setting the pace for the whole heart

Conduction pathway, in order

SA node -> (~0.1 sec delay) -> AV node -> AV bundle (Bundle of His) -> right & left bundle branches -> Purkinje (subendocardial conducting) fibers

Pacemaker potential (prepotential)

The unstable, slowly drifting resting membrane potential of pacemaker cells, caused by K+ channels staying closed while slow Na+ channels stay open

3 phases of the pacemaker cell action potential

1) Pacemaker potential (slow Na+ in, K+ closed) 2) Depolarization (Ca2+ channels open ~-40 mV) 3) Repolarization (K+ channels open, K+ efflux)

Cardiac contractile cell action potential: plateau phase

Caused by slow Ca2+ channels opening, prolonging depolarization and sustaining contraction

Why does cardiac muscle have a long absolute refractory period?

It prevents summation/tetanic contractions, which would stop the heart's pumping action entirely

Arrhythmia

General term for an irregular heart rhythm -- bradycardia (slow) or tachycardia (fast)

Fibrillation

Rapid, out-of-phase, fluttering contractions with no effective pumping ("bag of worms")

Ectopic pacemaker (ectopic focus)

An abnormal site (not the SA node) driving the heart's rhythm; caused by SA node damage, caffeine, nicotine, electrolyte imbalance, hypoxia, drugs

Heart block

Interference in impulse transmission to the ventricles, most often from AV node damage

Backup pacemaker rates if SA node fails

AV node takes over at ~40-50 bpm; if that fails too, the bundle/Purkinje fibers fire at ~20-40 bpm

Extrinsic control of heart rate: brain center

The medulla oblongata routes central control via the ANS to the SA/AV nodes and myocardium

Medulla: cardioacceleratory vs. cardioinhibitory centers

Cardioacceleratory center -> sympathetic input (norepinephrine) increases HR/force; cardioinhibitory center -> parasympathetic input via vagus nerve (acetylcholine) decreases HR

ECG: what it measures

The sum of all electro-chemical (electrical) activity in the myocardium at any given moment

ECG: P wave

Atrial depolarization

ECG: QRS complex

Ventricular depolarization (atrial repolarization occurs at the same time, hidden within it)

ECG: T wave

Ventricular repolarization

ECG: P-R interval

Atrial depolarization plus the AV nodal delay, before ventricular depolarization starts

ECG: Q-T interval

Ventricular depolarization through the end of ventricular repolarization

ECG: S-T segment

The brief plateau between the end of ventricular depolarization and the start of ventricular repolarization

Cardiac cycle: isovolumetric contraction

Occurs right after the QRS complex; all 4 valves closed; ventricular pressure rises with no volume change

Cardiac cycle: ventricular ejection

Semilunar valves open once ventricular pressure exceeds arterial pressure; blood is ejected

Cardiac cycle: isovolumetric relaxation

Occurs right after the T wave; all 4 valves closed again; ventricular pressure falls with no volume change

Cardiac output (CO) formula

CO = Heart Rate x Stroke Volume (normal approx. 70 bpm x 70 mL/beat = 4.9 L/min)

Cardiac reserve

Maximal CO minus resting CO; averages 4-5x resting CO in most people, up to 7x in trained athletes

Stroke volume (SV) formula

SV = EDV - ESV

End Diastolic Volume (EDV)

Volume of blood in the ventricle after filling; ~120 mL

End Systolic Volume (ESV)

Volume of blood remaining in the ventricle after contraction; ~50 mL

Ejection fraction (approx.)

Each heartbeat ejects about 60% of the blood in the ventricle

3 factors regulating stroke volume

Preload, contractility, afterload

Preload

Degree of stretch of cardiac muscle fibers just before contraction; determined mainly by venous return; affects EDV

Frank-Starling law of the heart

A greater EDV (stretch) produces a greater stroke volume -- "Venous Return up -> EDV up -> SV up -> CO up"

Contractility

Contractile strength independent of muscle stretch; increased by sympathetic norepinephrine opening Ca2+ channels, boosting actin-myosin cross-bridges and lowering ESV

Positive inotropic agents

Glucagon, thyroxine, epinephrine, digitalis -- all increase contractility

Negative inotropic factors

Acidosis (excess H+), high extracellular K+, calcium channel blockers -- all reduce contractility

Afterload

The pressure the ventricles must overcome to eject blood (essentially arterial blood pressure); high afterload leaves more blood in the ventricle after each beat

Quick rule: preload vs. contractility/afterload

Preload affects EDV; contractility and afterload affect ESV

Chronotropic effect

A change in heart rate (as opposed to inotropic = change in contraction strength)

Bainbridge effect

An increase in venous return/EDV stretches the SA node directly, increasing heart rate

Vagal tone

The resting parasympathetic (vagus nerve) signal that keeps heart rate "under the brakes" at baseline

Other factors affecting heart rate

Hormones (epinephrine, thyroxine), ion levels (K+, Ca2+), body temperature, age/gender, body mass/blood volume, exercise, stress/illness

Vessel wall: 3 tunics, inner to outer

Tunica intima (endothelium + basement membrane + internal elastic lamina), tunica media (smooth muscle + elastic fibers, thickest layer), tunica adventitia/externa (elastic + collagen fibers)

Elastic (conducting) arteries

Nearest the heart; largest diameter (~1.5 cm lumen) and thickest walls; most elastic fibers; site of the Windkessel effect; lose elasticity with age

Windkessel effect

Elastic arteries stretch during systole (absorbing the pressure wave) and elastically recoil during diastole, helping move blood forward when the heart isn't pumping

Muscular (distributing) arteries

Deliver blood to organs; smaller lumen (~6.0 mm) than elastic arteries; more smooth muscle, fewer elastic fibers, more active vasoconstriction

Arterioles

Regulate flow into capillary beds; tiny lumen (~37 micrometers); dominated by smooth muscle; the main site of blood pressure regulation via vasoconstriction

Microcirculation

The exchange region between arteries and veins; capillary density is higher in tissues with higher metabolic activity (e.g., skeletal muscle)

Continuous capillaries

Most common type; continuous endothelium with intercellular clefts (tight junctions in the brain form the blood-brain barrier); found in skin, muscle, CNS

Fenestrated capillaries

Have "window" pores for fast fluid exchange; found in kidney glomeruli, small intestine, endocrine glands

Sinusoid capillaries

Widest, most permeable, irregular lumen, incomplete basement membrane; allow large molecules/cells through; found in liver, bone marrow, spleen

Capillary exchange mechanisms

Lipid-soluble molecules diffuse through the membrane directly; small water-soluble molecules pass through clefts/fenestrations; large molecules need vesicular transport

Venules

Collect blood from capillary beds; become more vessel-like (more smooth muscle/connective tissue) farther from the capillaries

Veins: structural traits

Thinner walls, larger lumen (~5.0 mm) than corresponding arteries; thin tunica media, thick tunica externa; have valves; high compliance; low pressure

Varicose veins

Caused by incompetent (leaky) valves or elevated venous pressure, making veins tortuous and dilated

At-rest blood distribution

~60% of total blood volume sits in the veins and venules, which act as a volume/blood reservoir

Resting vs. exercising blood flow shifts

At rest, skeletal muscle gets ~1200 mL/min; during vigorous exercise, that jumps to ~12,500 mL/min, mostly at the expense of the kidneys/abdomen; brain flow stays constant (~750 mL/min) in both states

Flow equation

Flow = Delta-P / R (pressure difference over resistance)

Flow as cardiac output

CO = MAP / R (mean arterial pressure over resistance)

Resistance & viscosity

Resistance is directly proportional to blood viscosity ("thickness") -- increased by dehydration, polycythemia, or excess plasma proteins

Resistance & vessel length

Resistance is directly proportional to vessel length (e.g., obesity increases total vessel length needed)

Resistance & radius

Resistance is inversely proportional to radius to the 4th power -- halving the radius increases resistance 16-fold

Total Peripheral Resistance (TPR) / Systemic Vascular Resistance (SVR)

All resistance offered by the systemic vessels combined; highest in the arterioles, which also cause the single largest pressure drop

Pulse pressure

Systolic pressure minus diastolic pressure

Mean Arterial Pressure (MAP) formula

MAP = diastolic pressure + (pulse pressure / 3), equivalently (systolic + 2 x diastolic) / 3

Effect of the Windkessel effect on pulse pressure

Decreases pulse pressure (smooths out the pressure spike)

Effect of arterial hardening (atherosclerosis) on pulse pressure

Increases pulse pressure (stiff vessels can't absorb/smooth the systolic surge)